Alves, Frauke

[["dc.bibliographiccitation.journal","Journal of Investigative Dermatology"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Mueller-Homey, Anja"],["dc.contributor.author","Seeliger, Stefan"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Buhren, Bettina Alexandra"],["dc.contributor.author","Sleeman, Jonathan"],["dc.contributor.author","Stoecklein, Nikolas H."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Hoffmann, Thomas"],["dc.contributor.author","Homey, Bernhard"],["dc.date.accessioned","2018-11-07T08:39:51Z"],["dc.date.available","2018-11-07T08:39:51Z"],["dc.date.issued","2010"],["dc.format.extent","S51"],["dc.identifier.isi","000281110100300"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19099"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.publisher.place","New york"],["dc.relation.eventlocation","Helsinki, FINLAND"],["dc.relation.issn","0022-202X"],["dc.title","Tumor derived CCL20 production critically contributes to angiogenesis and tumor progression"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","942"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","British Journal of Cancer"],["dc.bibliographiccitation.lastpage","954"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Braun, Stephan Alexander"],["dc.contributor.author","Oláh, Péter"],["dc.contributor.author","Gerber, Peter Arne"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Seeliger, Stephan"],["dc.contributor.author","Holtz, Stephanie"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Pivarcsi, Andor"],["dc.contributor.author","Buhren, Bettina"],["dc.contributor.author","Schrumpf, Holger"],["dc.contributor.author","Kislat, Andreas"],["dc.contributor.author","Bünemann, Erich"],["dc.contributor.author","Steinhoff, Martin"],["dc.contributor.author","Fischer, Jens"],["dc.contributor.author","Lira, Sérgio A."],["dc.contributor.author","Boukamp, Petra"],["dc.contributor.author","Hevezi, Peter"],["dc.contributor.author","Stoecklein, Nikolas Hendrik"],["dc.contributor.author","Hoffmann, Thomas"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Sleeman, Jonathan"],["dc.contributor.author","Bauer, Thomas"],["dc.contributor.author","Klufa, Jörg"],["dc.contributor.author","Amberg, Nicole"],["dc.contributor.author","Sibilia, Maria"],["dc.contributor.author","Zlotnik, Albert"],["dc.contributor.author","Müller-Homey, Anja"],["dc.contributor.author","Homey, Bernhard"],["dc.date.accessioned","2021-04-14T08:25:49Z"],["dc.date.available","2021-04-14T08:25:49Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41416-020-0943-2"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81742"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1532-1827"],["dc.relation.haserratum","/handle/2/103504"],["dc.relation.issn","0007-0920"],["dc.title","EGFR/Ras-induced CCL20 production modulates the tumour microenvironment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","30"],["dc.bibliographiccitation.journal","Molecular Cancer"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Twarock, Soeren"],["dc.contributor.author","Freudenberger, Till"],["dc.contributor.author","Poscher, Eva"],["dc.contributor.author","Dai, Guang"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Prenzel, Klaus"],["dc.contributor.author","Knoefel, Wolfram Trudo"],["dc.contributor.author","Stoecklein, Nikolas H."],["dc.contributor.author","Savani, Rashmin C."],["dc.contributor.author","Homey, Bernhard"],["dc.contributor.author","Fischer, Jens W."],["dc.date.accessioned","2018-11-07T08:58:01Z"],["dc.date.available","2018-11-07T08:58:01Z"],["dc.date.issued","2011"],["dc.description.abstract","Background: Oesophageal cancer is a highly aggressive tumour entity with at present poor prognosis. Therefore, novel treatment options are urgently needed. Hyaluronan (HA) is a polysaccharide present in the matrix of human oesophageal squamous cell carcinoma (ESCC). Importantly, in vitro ESCC cells critically depend on HA synthesis to maintain the proliferative phenotype. The aim of the present study is (1) to study HA-synthase (HAS) expression and regulation in human ESCC, and (2) to translate the in vitro results into a mouse xenograft model of human ESCC to study the effects of systemic versus tumour targeted HAS inhibition on proliferation and distribution of tumour-bound and stromal hyaluronan. Methods: mRNA expression was investigated in human ESCC biopsies by semiquantitative real-time RT PCR. Furthermore, human ESCC were xenografted into NMRI nu/nu mice. The effects on tumour progression and morphology of 4-methylumbelliferone (4-MU), an inhibitor of HA-synthesis, and of lentiviral knock down of HA-synthase 3 (HAS3), the main HAS isoform in the human ESCC tissues and the human ESCC cell line used in this study, were determined. Tumour progression was monitored by calliper measurements and by flat-panel detector volume computed tomography (fpVCT). HA content, cellular composition and proliferation (Ki67) were determined histologically. Results: mRNA of HAS isoform 3 (HAS3) was upregulated in human ESCC biopsies and HAS3 mRNA was positively correlated to expression of the epidermal growth factor (EGF) receptor. EGF was also proven to be a strong inductor of HAS3 mRNA expression in vitro. During the course of seven weeks, 4-MU inhibited progression of xenograft tumours. Interestingly, remodelling of the tumour into a more differentiated phenotype and inhibition of cell proliferation were observed. Lentiviral knockdown of HAS3 in human ESCC cells prior to xenografting mimicked all effects of 4-MU treatment suggesting that hyaluronan produced by ESCC is accountable for major changes in tumour environment in vivo. Conclusions: Systemic inhibition of HA-synthesis and knockdown of tumour cell HAS3 cause decreased ESCC progression accompanied by tumour stroma remodelling and may therefore be used in novel approaches to ESCC therapy."],["dc.identifier.doi","10.1186/1476-4598-10-30"],["dc.identifier.isi","000289648500001"],["dc.identifier.pmid","21429221"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6168"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23544"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1476-4598"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Inhibition of Oesophageal Squamous Cell Carcinoma Progression by in vivo Targeting of Hyaluronan Synthesis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4275"],["dc.bibliographiccitation.issue","41"],["dc.bibliographiccitation.journal","Oncogene"],["dc.bibliographiccitation.lastpage","4288"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Gerstel, Daniela"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Ludewig, P."],["dc.contributor.author","Scheike, K."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Beauchemin, Nicole"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Wagener, Christoph"],["dc.contributor.author","Horst, Andrea Kristina"],["dc.date.accessioned","2018-11-07T08:51:04Z"],["dc.date.available","2018-11-07T08:51:04Z"],["dc.date.issued","2011"],["dc.description.abstract","We have studied the effects of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) on tumor angiogenesis in murine ductal mammary adenocarcinomas. We crossed transgenic mice with whey acidic protein promoter-driven large T-antigen expression (WAP-T mice) with oncogene-induced mammary carcinogenesis with CEA-CAM1null mice, and with Tie2-Ceacam1 transgenics, in which the Tie2 promoter drives endothelial overexpression of CEACAM1 (WAP-T x CEACAM1(endo+) mice), and analyzed tumor vascularization, angiogenesis and vessel maturation in these mice. Using flat-panel volume computed tomography (fpVCT) and histology, we found that WAP-T x CEACAM1(endo+) mice exhibited enhanced tumoral vascularization owing to CEACAM1(+) vessels in the tumor periphery, and increased intratumoral angiogenesis compared with controls. In contrast, vascularization of CEACAM1null/WAP-T-derived tumors was poor, and tumor vessels were dilated, leaky and showed poor pericyte coverage. Consequently, the tumoral vasculature could not be visualized in CEACAM1null/WAP-T mice by fpVCT, and we observed poor organization of the perivascular extracellular matrix (ECM), accompanied by the accumulation of collagen IV-degrading matrix metalloproteinase 9(+) (MMP9(+)) leukocytes and stromal cells. Vascular instability and alterations in ECM structure were accompanied by a significant increase in pulmonary metastases in CEACAM1null/WAP-T mice, whereas only occasional metastases were observed in CEACAM1(+) hosts. In CEACAM1(+) hosts, intratumoral vessels did not express CEACAM1, but they were intact, extensively covered with pericytes and framed by a well-organized perivascular ECM. MMP9(+) accessory cells were largely absent. Orthotopic transplantation of primary WAP-T- and CEACAM1null/WAP-T tumors into all three mouse lines confirmed that a CEACAM1(+) host environment is a prerequisite for productive angiogenic remodeling of the tumor microenvironment. Hence, CEACAM1 expression in the tumor periphery determines the vascular phenotype in a tumor, whereas systemic absence of CEACAM1 interferes with the formation of an organized tumor matrix and intratumoral vessel maturation. Oncogene (2011) 30, 4275-4288; doi: 10.1038/onc.2011.146; published online 2 May 2011"],["dc.description.sponsorship","German Research Foundation [SPP1190]"],["dc.identifier.doi","10.1038/onc.2011.146"],["dc.identifier.isi","000296356300005"],["dc.identifier.pmid","21532628"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21845"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0950-9232"],["dc.title","CEACAM1 creates a pro-angiogenic tumor microenvironment that supports tumor vessel maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","25"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","137"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Lenfert, Eva"],["dc.contributor.author","Maenz, Claudia"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T09:55:37Z"],["dc.date.available","2018-11-07T09:55:37Z"],["dc.date.issued","2015"],["dc.description.abstract","In this study, the effects of the standard chemotherapy, cyclophosphamide/adriamycin/5-fluorouracil (CAF) on tumor growth, dissemination and recurrence after orthotopic implantation of murine G-2 cells were analyzed in the syngeneic immunocompetent whey acidic protein-T mouse model (Wegwitz et al., PLoS One 2010; 5:e12103; Schulze-Garg et al., Oncogene 2000; 19:1028-37). Single-dose CAF treatment reduced tumor size significantly, but was not able to eradicate all tumor cells, as recurrent tumor growth was observed 4 weeks after CAF treatment. Nine days after CAF treatment, residual tumors showed features of regressive alterations and were composed of mesenchymal-like tumor cells, infiltrating immune cells and some tumor-associated fibroblasts with an intense deposition of collagen. Recurrent tumors were characterized by coagulative necrosis and less tumor cell differentiation compared with untreated tumors, suggesting a more aggressive tumor phenotype. In support, tumor cell dissemination was strongly enhanced in mice that had developed recurrent tumors in comparison with untreated controls, although only few disseminated tumor cells could be detected in various organs 9 days after CAF application. In vitro experiments revealed that CAF treatment of G-2 cells eliminates the vast majority of epithelial tumor cells, whereas tumor cells with a mesenchymal phenotype survive. These results together with the in vivo findings suggest that tumor cells that underwent epithelial-mesenchymal transition and/or exhibit stem-cell-like properties are difficult to eliminate using one round of CAF chemotherapy. The model system described here provides a valuable tool for the characterization of the effects of chemotherapeutic regimens on recurrent tumor growth and on tumor cell dissemination, thereby enabling the development and preclinical evaluation of novel therapeutic strategies to target mammary carcinomas."],["dc.identifier.doi","10.1002/ijc.29369"],["dc.identifier.isi","000353297600003"],["dc.identifier.pmid","25449528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36792"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1097-0215"],["dc.relation.issn","0020-7136"],["dc.title","Chemotherapy of WAP-T mouse mammary carcinomas aggravates tumor phenotype and enhances tumor cell dissemination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Experimental Dermatology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Hippe, Andreas"],["dc.contributor.author","Schorr, Anne"],["dc.contributor.author","Mueller-Horney, A."],["dc.contributor.author","Lierop, A. van"],["dc.contributor.author","Steinhoff, Martin"],["dc.contributor.author","Seeliger, Stefan"],["dc.contributor.author","Kubitza, R."],["dc.contributor.author","Buenemann, E."],["dc.contributor.author","Liersch, Ruediger"],["dc.contributor.author","Heroult, M."],["dc.contributor.author","Hoffmann, T. K."],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Brema, S."],["dc.contributor.author","Boukamp, P."],["dc.contributor.author","Mueller, M."],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Sleeman, J. P."],["dc.contributor.author","Augustin, H."],["dc.contributor.author","Zlotnik, A."],["dc.contributor.author","Horney, B."],["dc.date.accessioned","2018-11-07T08:32:02Z"],["dc.date.available","2018-11-07T08:32:02Z"],["dc.date.issued","2009"],["dc.identifier.isi","000263520200222"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17255"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.eventlocation","Heidelberg, GERMANY"],["dc.title","The role of the chemokine CCL20 in tumor-associated angiogenesis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","513"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Gastroenterology"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Matzke-Ogi, Alexandra"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Shatirishvili, Marine"],["dc.contributor.author","Fuchs, Beatrix"],["dc.contributor.author","Chiblak, Sara"],["dc.contributor.author","Morton, Jennifer"],["dc.contributor.author","Tawk, Bouchra"],["dc.contributor.author","Lindner, Thomas"],["dc.contributor.author","Sansom, Owen"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Warth, Arne"],["dc.contributor.author","Schwager, Christian"],["dc.contributor.author","Mier, Walter"],["dc.contributor.author","Kleeff, Joerg"],["dc.contributor.author","Ponta, Helmut"],["dc.contributor.author","Abdollahi, Amir"],["dc.contributor.author","Orian-Rousseau, Veronique"],["dc.date.accessioned","2018-11-07T10:18:53Z"],["dc.date.available","2018-11-07T10:18:53Z"],["dc.date.issued","2016"],["dc.description.abstract","BACKGROUND & AIMS: Cancer cells with high metastatic potential and stem cell-like characteristics express the cell surface marker CD44. CD44 isoforms that include the v6 exon are co-receptors for the receptor tyrosine kinases MET and Vascular Endothelial Growth factor Receptor-2 (VEGFR2). We studied CD44v6 signaling in several pancreatic cancer cell lines, and its role in tumor growth and metastasis in several models of pancreatic cancer. METHODS: We analyzed the effects of v6 peptides that interfere with the co-receptor functions of CD44v6 for MET and VEGFR-2 in tumors and metastases grown from cells that express different CD44 isoforms, including CD44v6. The peptides were injected into rats with syngeneic tumors and mice with orthotopic or xenograft tumors. We also tested the effects of the peptides in mice with xenograft tumors grown from patient tumor samples and mice that express an oncogenic form of RAS and develop spontaneous pancreatic cancer (KPC mice). We measured levels of CD44v6 messenger RNA (mRNA) in pancreatic cancer tissues from 136 patients. RESULTS: Xenograft tumors grown from human cancer cells injected with v6 peptides were smaller and formed fewer metastases in mice. The v6 peptide was more efficient than the MET inhibitor crizotinib and/or the VEGFR-2 inhibitor pazopanib in reducing xenograft tumor growth and metastasis. Injection of KPC mice with the v6 peptide increased their survival time. Injection of mice and rats bearing metastases with the v6 peptide induced regression of metastases. Higher levels of CD44v6 mRNA in human pancreatic tumor tissues were associated with increased expression of MET, tumor metastasis, and shorter patient survival times. CONCLUSIONS: Peptide inhibitors of CD44v6 isoforms block tumor growth and metastasis in several independent models of pancreatic cancer. The v6 peptides induced regression of metastases. Levels of CD44v6 mRNA are increased, along with those of MET mRNA, in patients with metastatic pancreatic tumors, compared with nonmetastatic tumors; the increased levels correlated with shorter patient survival time."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [OR 124/4-1, OR 124/4-2]"],["dc.identifier.doi","10.1053/j.gastro.2015.10.020"],["dc.identifier.isi","000368629900037"],["dc.identifier.pmid","26597578"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41544"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","1528-0012"],["dc.relation.issn","0016-5085"],["dc.title","Inhibition of Tumor Growth and Metastasis in Pancreatic Cancer Models by Interference With CD44v6 Signaling"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","62"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Cancer"],["dc.bibliographiccitation.lastpage","70"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Heinlein, Christina"],["dc.contributor.author","Krepulat, Frauke"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Deppert, Wolfgang R."],["dc.contributor.author","Alves, Frauke"],["dc.date.accessioned","2018-11-07T08:28:11Z"],["dc.date.available","2018-11-07T08:28:11Z"],["dc.date.issued","2009"],["dc.description.abstract","Transgenic mouse models offer an excellent opportunity for studying the molecular basis of cancer development and progression. Here we applied flat-panel volume computed tomography (fpVCT) to monitor tumor progression as well as the development of tumor vasculature in vivo in a transgenic mouse model for oncogene-induced mammary carcinogenesis (WAP-T mice). WAP-T mice develop multiple mammary carcinomas on oncogene induction within 3 to 5 months. Following induction, 3-dimensional fpVCT data sets were obtained by serial single scans of entire mice in combination with iodine containing contrast agents and served as basis for precise measurements of tumor volumes. Thereby, we were able to depict tumors within the mammary glands at a very early stage of the development. Tumors of small sizes (0.001 cm(3)) were detected by fpVCT before being palpable or visible by inspection. The capability to determine early tumor onset combined with longitudinal noninvasive imaging identified diverse time points of tumor onset for each mammary carcinoma and different tumor growth kinetics for multiple breast carcinomas that developed in single mice. Furthermore, blood supply to the breast tumors, as well as blood vessels around and within the tumors, were clearly visible over time by fpVCT. Three-dimensional visualization of tumor vessels in high resolution was enhanced by the use of a novel blood pool contrast agent. Here, we demonstrate by longitudinal fpVCT imaging that mammary carcinomas develop at different time points in each WAP-T mouse, and thereafter show divergent growth rates and distinct vascularization patterns. (C) 2009 UICC"],["dc.identifier.doi","10.1002/ijc.24332"],["dc.identifier.isi","000266569200008"],["dc.identifier.pmid","19384954"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6325"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16366"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0020-7136"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Detection of different tumor growth kinetics in single transgenic mice with oncogene-induced mammary carcinomas by flat-panel volume computed tomography"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","254"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neoplasia"],["dc.bibliographiccitation.lastpage","263"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Schneider, Manuela"],["dc.contributor.author","Wortmann, Markus"],["dc.contributor.author","Mandal, Pankaj Kumar"],["dc.contributor.author","Arpornchayanon, Warangkana"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Strieth, Sebastian"],["dc.contributor.author","Conrad, Marcus"],["dc.contributor.author","Beck, Heike"],["dc.date.accessioned","2022-03-01T11:44:19Z"],["dc.date.available","2022-03-01T11:44:19Z"],["dc.date.issued","2010"],["dc.description.abstract","The selenoenzyme glutathione peroxidase 4 (GPx4) has been described to control specific cyclooxygenases (COXs) and lipoxygenases (LOXs) that exert substantiated functions in tumor growth and angiogenesis. Therefore, we hypothesized a putative regulatory role of GPx4 during tumor progression and created transformed murine embryonic fibroblasts with inducible disruption of GPx4. GPx4 inactivation caused rapid cell death in vitro, which could be prevented either by lipophilic antioxidants or by 12/15-LOX-specific inhibitors, but not by inhibitors targeting other LOX isoforms or COX. Surprisingly, transformed GPx4(+/-) cells did not die when grown in Matrigel but gave rise to tumor spheroids. Subcutaneous implantation of tumor cells into mice resulted in knockout tumors that were indistinguishable in volume and mass in comparison to wild-type tumors. However, further analysis revealed a strong vascular phenotype. We observed an increase in microvessel density as well as a reduction in the number of large diameter vessels covered by smooth muscle cells. This phenotype could be linked to increased 12/15-LOX activity that was accompanied by an up-regulation of basic fibroblast growth factor and down-regulation of vascular endothelial growth factor A protein expression. Indeed, pharmacological inhibition of 12/15-LOX successfully reversed the tumor phenotype and led to \"normalized\" vessel morphology. Thus, we conclude that GPx4, through controlling 12/15-LOX activity, is an important regulator of tumor angiogenesis as well as vessel maturation."],["dc.identifier.doi","10.1593/neo.91782"],["dc.identifier.fs","567900"],["dc.identifier.pii","S1476558610801046"],["dc.identifier.pmid","20234819"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6890"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/102992"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","1476-5586"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.mesh","Animals"],["dc.subject.mesh","Apoptosis"],["dc.subject.mesh","Arachidonate 12-Lipoxygenase"],["dc.subject.mesh","Arachidonate 15-Lipoxygenase"],["dc.subject.mesh","Blotting, Western"],["dc.subject.mesh","Cell Adhesion"],["dc.subject.mesh","Cell Culture Techniques"],["dc.subject.mesh","Cell Movement"],["dc.subject.mesh","Cell Proliferation"],["dc.subject.mesh","Cell Transformation, Neoplastic"],["dc.subject.mesh","Embryo, Mammalian"],["dc.subject.mesh","Enzyme-Linked Immunosorbent Assay"],["dc.subject.mesh","Extracellular Matrix"],["dc.subject.mesh","Fibroblast Growth Factor 2"],["dc.subject.mesh","Fibroblasts"],["dc.subject.mesh","Fluorescent Antibody Technique"],["dc.subject.mesh","Genes, ras"],["dc.subject.mesh","Glutathione Peroxidase"],["dc.subject.mesh","Immunoenzyme Techniques"],["dc.subject.mesh","Mice"],["dc.subject.mesh","Mice, Inbred C57BL"],["dc.subject.mesh","Mice, Knockout"],["dc.subject.mesh","Mice, SCID"],["dc.subject.mesh","Neoplasms, Experimental"],["dc.subject.mesh","Neovascularization, Pathologic"],["dc.subject.mesh","Pregnancy Proteins"],["dc.subject.mesh","Proto-Oncogene Proteins c-myc"],["dc.subject.mesh","RNA, Messenger"],["dc.subject.mesh","Reverse Transcriptase Polymerase Chain Reaction"],["dc.subject.mesh","Spheroids, Cellular"],["dc.subject.mesh","Vascular Endothelial Growth Factor A"],["dc.title","Absence of Glutathione Peroxidase 4 Affects Tumor Angiogenesis through Increased 12/15-Lipoxygenase Activity"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","286"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Radiology"],["dc.bibliographiccitation.lastpage","293"],["dc.bibliographiccitation.volume","70"],["dc.contributor.author","Alves, Frauke"],["dc.contributor.author","Dullin, Christian"],["dc.contributor.author","Napp, Joanna"],["dc.contributor.author","Missbach-Guentner, Jeannine"],["dc.contributor.author","Jannasch, Katharina"],["dc.contributor.author","Mathejczyk, Julia"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Tietze, Lutz Friedjan"],["dc.date.accessioned","2018-11-07T08:30:16Z"],["dc.date.available","2018-11-07T08:30:16Z"],["dc.date.issued","2009"],["dc.description.abstract","Conventional chemotherapy of cancer has its limitations, especially in advanced and disseminated disease and suffers from lack of specificity. This results in a poor therapeutic index and considerable toxicity to normal organs. Therefore, many efforts are made to develop novel therapeutic tools against cancer with the aim of selectively targeting the drug to the turnout site. Drug delivery strategies fundamentally rely on the identification of good-quality biomarkers, allowing unequivocal discrimination between cancer and healthy tissue. At present, antibodies or antibody fragments have clearly proven their value as carrier molecules specific for a tumour-associated molecular marker. This present review draws attention to the use of near-infrared fluorescence (NIRF) imaging to investigate binding specificity and kinetics of carrier molecules such as monoclonal antibodies. In addition, flat-panel volume computed tomography (fpVCT) will be presented to monitor anatomical structures in turnout mouse models over time in a non-invasive manner. Each imaging device sheds light on a different aspect; functional imaging is applied to optimise the dose schedule and the concept of selective tumour therapies, whereas anatomical imaging assesses preclinically the efficacy of novel turnout therapies. Both imaging techniques in combination allow the visualisation of functional information obtained by NIRF imaging within an adequate anatomic framework. (C) 2009 Elsevier Ireland Ltd. All rights reserved."],["dc.description.sponsorship","DFG [SFB 416, AL336/5-1]"],["dc.identifier.doi","10.1016/j.ejrad.2009.01.048"],["dc.identifier.isi","000266868900012"],["dc.identifier.pmid","19285818"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16849"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0720-048X"],["dc.title","Concept of a selective tumour therapy and its evaluation by near-infrared fluorescence imaging and flat-panel volume computed tomography in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]